Throughout this application various publications are referenced, many in parentheses, with full citations in the references section. The disclosures of each of these publications in their entireties are hereby incorporated by reference in this application.
Respiratory syncytial virus (RSV) is an enveloped, negative-sense single-stranded RNA virus (1). Since its isolation, RSV has been identified as a leading cause of epidemic respiratory tract illness in children in the U.S. and worldwide. In fact, RSV is so ubiquitous that it will infect 100% of children before the age of 3. It is estimated that 40-50% of children hospitalized with bronchiolitis and 25% of children with pneumonia are infected with RSV, resulting in 100,000 hospital admissions annually in the US alone (1). In addition to acute morbidity, there are long-term consequences of RSV infection in infancy. RSV has been shown to predispose to the development of hyperreactive airway disease (2) and recurrent episodes of wheezing in asthmatic children are often precipitated by RSV infection. The mechanisms of RSV-induced airway disease and its long-term consequences are largely unknown, but the delicate balance between immunopathology and immunoprotection in the airway mucosa may be altered by an exuberant and unwanted local inflammatory response. Airway infiltration of monocytes and lymphocytes is typical of RSV infection (1), and activation of eosinophil and basophil leukocytes has been shown to correlate with the severity of acute RSV disease (3;4).